Effects Of Various Prostaglandins Research Articles

Contractile Efficacy of Various Prostaglandins in Pregnant Rat Myometrium Pretreated With Oxytocin

Oxytocin pretreatment of pregnant rat myometrium has been shown to reduce the contractions produced by further administration of oxytocin, as a function of the desensitization phenomenon. It is unclear whether this phenomenon affects the contractions produced by various prostaglandins that are used in the management of postpartum hemorrhage. The objective of this study was to investigate the contractile effects of various prostaglandins after oxytocin pretreatment and to compare their relative efficacies in vitro on pregnant rat myometrial strips. Myometrial samples from 29 pregnant Wistar rats at term were isolated and pretreated with oxytocin (10(-8) mol/L, experimental group) or physiological salt solution (control group) for 1 hour. They were then subjected to dose-response testing with oxytocin (n = 32), PGF2α (n = 16), dinoprostone (n = 14), alprostadil (n = 14), or misoprostol (n = 15) with cumulative increases in the organ bath concentrations from 10(-10) to 10(-5) mol/L. The contractile efficacies of various prostaglandins and oxytocin during the dose response were analyzed using mixed linear modeling and compared between the groups. There was no significant difference in the amplitude, frequency, motility index (amplitude × frequency), or area under the curve of all prostaglandins between the groups pretreated with oxytocin and the control group. However, there was a significant decrease in the frequency (P = .02) and motility index (P = .05) in the dose-response curves of oxytocin in the groups pretreated with oxytocin compared with the control groups. Overall, oxytocin produced superior contractions compared with all other prostaglandins, while dinoprostone and misoprostol produced the weakest contractions. The uterotonic effects of various prostaglandins are not affected by oxytocin desensitization; and despite desensitization, oxytocin provides superior contractions compared with the prostaglandins.

Effect of various prostaglandins on the metabolism of fructose by epididymal and ejaculated ram spermatozoa in vitro.

The effects of a number of prostaglandins on the metabolism of fructose by epididymal and ejaculated ram spermatozoa were investigated using conventional Warburg techniques. Spermatozoa from the two sources were collected concurrently during electrical stimulation; the epididymal spermatozoa were harvested via a cannula inserted chronically into one vas deferens and thus were free from exposure to the seminal prostaglandins. In general, the metabolism of fructose by the spermatozoa was little affected by a wide range of prostaglandins at a concentration of 20 micrograms/ml. Of the PGs present in semen, PGE2, PGE3 and PGF2alpha had no significant effects whereas PGE1 and PGF1alpha significantly increased lactate accumulation and the latter increased oxygen uptake, in both cases without significantly changing fructose utilization, fructose oxidized or CO2 production. Both 15-methyl-substituted PGE2 and PGF2alpha and their corresponding methyl esters failed to change fructose metabolism and it is unlikely therefore that the lack of response to PGE2 and PGF2alpha was due to their being metabolized by the spermatozoa during the incubation. Of a number of breakdown products tested, PGA1 and to a lesser extent PGA2 appeared to inhibit the Krebs tricarbocyclic acid cycle and 15-keto 13,14-dihydro-PGF2alpha appeared to stimulate it. In general, epididymal spermatozoa responded to the PGs in the same way as ejaculated spermatozoa. Thus we did not confirm a suggestion in the literature that spermatozoa have lowered sensitivity to PGs in vitro once they have been in contact with the PGs in seminal plasma.

Cyclooxygenase-2 and prostaglandin F2 alpha in Syrian hamster Leydig cells: Inhibitory role on luteinizing hormone/human chorionic gonadotropin-stimulated testosterone production.

We have previously found that cyclooxygenase-2 (COX-2), a key enzyme in the biosynthesis of prostaglandins (PGs), is present in the testicular interstitial cells of infertile men, whereas it is absent in human testes with no evident morphological changes or abnormalities. To find an animal model for further investigating COX-2 and its role in testicular steroidogenesis, we screened testes from adult species ranging from mice to monkeys. By using immunohistochemical assays, we found COX-2 expression only in Leydig cells of the reproductively active (peripubertal, pubertal, and adult) seasonal breeder Syrian hamster. COX-2 expression in hamster Leydig cells was confirmed by RT-PCR. In contrast, COX-1 expression was not detected in hamster testes. Because COX-2 expression implies PG synthesis, we investigated the effect of various PGs on testosterone production and found that PGF2 alpha stood out because it significantly reduced human chorionic gonadotropin-stimulated testosterone release from isolated hamster Leydig cells in a dose-dependent manner. This mechanism involves a decreased expression of testicular steroidogenic acute regulatory protein and 17beta-hydroxysteroid dehydrogenase. Testicular concentration and content of PGF2 alpha in reproductively active hamsters as well as production of PGF2 alpha from isolated hamster Leydig cells were also determined. Moreover, PGF2 alpha receptors were localized in Leydig cells of hamsters and testicular biopsies from patients with Sertoli cell only and germ arrest syndromes. Thus, in this study, we described a COX-2-initiated pathway that via PGF2 alpha production, PGF2 alpha receptors, steroidogenic acute regulatory protein, and 17beta-hydroxysteroid dehydrogenase represents a physiological local inhibitory system of human chorionic gonadotropin-stimulated testosterone production in the Syrian hamster testes.

Effect of prostaglandins against alloxan-induced cytotoxicity to insulin secreting insulinoma RIN cells in vitro

In the present study, we studied the effect of various prostaglandins (PGs) on alloxan-induced cytotoxicity to rat insulinoma (RIN) cells. Of all the PGs tested, PGE1, PGE2, PGI2, PGF1α, and PGF3α protected RIN cells from alloxan-induced cytotoxicity (P<0.05 compared to alloxan), whereas thromboxane B2 and 6-keto-PGF1α were not effective. PGE1 induces a statistically significant increase in the activities of superoxide dismutase and glutathione peroxidase and decrease in lipid peroxides in alloxan-treated RIN cells (P<0.001). PGE1 restored nitric oxide/lipid peroxide ratio to normalcy, suggesting that PGE1 suppresses oxidant stress induced by alloxan in RIN cells in vitro. Furthermore, PGE1 prevented DNA damage and apoptosis induced by alloxan. These results indicate that PGE1 prevents alloxan-induced cytotoxicity to RIN cells in vitro.

Effect of Prostaglandins A2, E1, F2 αand Latanoprost on Cultured Human Iridal Melanocytes

The effect of various prostaglandins on the growth, melanogenesis and dendrification of cultured iridal melanocytes were studied. Iridal melanocytes were isolated and cultured with medium supplemented with cAMP elevating agents and basic fibroblast growth factor (complete medium). The iridal melanocytes were plated into multiple well plates and cultured with complete medium, cAMP-deleted medium with or without various prostaglandins at different concentrations. After 5–7 days, the numbers of cells and dendrites were counted and melanin content was measured and compared to controls. Prostaglandin A2and E1stimulated growth, melanogenesis and dendrification of cultured iridal melanocytes in cAMP-deleted medium. Prostaglandin F2 α, PhXA85 and latanoprost showed no effect under similar experimental conditions. These results indicate that prostaglandin A2and E1stimulate growth and differentiation of iridal melanocytes through the activation of cAMP system. Failure of stimulation of melanogenesis of iridal melanocytes by prostaglandin F2 αand PhXA85 in vitro may be related to a different second messenger system activated by these prostaglandins and the selective stimulating effect of these prostaglandins on iridal melanocytes from mixed-colored irides.

In vitro effects of nonsteroidal anti-inflammatory agents and prostaglandins I2, E2, and F2α on contractility of taenia of the large colon of horses

Abstract Objectives To determine the in vitro effect of various prostaglandins (PG) and nonsteroidal anti-inflammatory drugs (NSAID) on contractile activity of the large-colon taenia of horses. Animals 14 healthy horses. Procedure The taenia was collected from the ventral colon, cut into strips (2 × 10 mm), and mounted in a tissue bath system (20-ml capacity) that contained oxygenated Krebs buffer solution warmed to 37.5 ± 0.5 C. After equilibration, incremental doses of PGE2, PGF2α, PGI2, flunixin meglumine, carprofen, ketoprofen, and phenylbutazone were added to the baths, and contractile activity was recorded. Magnitude of the response was calculated by comparing contractile activity before and after administration of the PG or NSAID to the tissue baths. Results PGE2 and PGF2α caused a significant increase in contractile activity, whereas PGL2 induced an inhibitory response. Activity of NSAID on contraction was predominantly inhibitory. At low concentrations, ketoprofen induced an excitatory effect, which then became inhibitory at high concentrations. Compared with the other NSAID, carprofen significantly reduced contractile activity at lower concentrations. Conclusions PGE2 and PGF2α appear to enhance contractility of large-colon taenia of horses, whereas PGL2 was inhibitory in the in vitro model. Administration of NSAID also inhibited contractility, with carprofen having the most potent effect. Clinical Relevance Administration of NSAID in combination with liberation of endogenous PG may predispose horses to development of intestinal stasis and subsequent impaction. (Am J Vet Res 1999;60:1004-1009)

Response of human gingival fibroblasts to prostaglandins.

The effects of various prostaglandins (PGs) on the functions of human gingival fibroblasts (Gin-1 cells; ATCC CRL 1292) were examined by phase-contrast microscopy, cell-counting and radioautographic experiments. Tested PGs were PGA1, PGA2, PGB1, PGB2, PGD2, PGE1, PGE2, PGF1 alpha, PGF2 alpha, PGI2, 6-keto-PGF1 alpha, 9 alpha-11 alpha-methanoepoxy-PGF2 alpha, and thromboxane (TX) B2. PGA1 and PGD2 at 30 microM caused morphological deformation of Gin-1 cells. All the PGs tested at 30 microM suppressed the proliferation of Gin-1 cells in the logarithmic growth phase. Furthermore, all the PGs tested at 10 microM suppressed DNA synthesis, collagen synthesis, and noncollagenous protein synthesis in confluent Gin-1 cells, while exerting no effect on GAG synthesis. The concentrations of PGs used are beyond those found in healthy gingiva. However, in periodontitis the local concentrations of some PGs within the gingiva are expected to be extremely elevated beyond the physiological level. These results suggest that PGs may play an important role as a negative regulator in metabolism and some pathologic gingival conditions by suppressing the functions of gingival fibroblasts.

Mechanism of inhibitory action of prostaglandins on the growth of human gastric carcinoma cell line KATO III

Prostaglandins (PGs) play important roles in the regulation of various gastric functions. In this study, the effects of various PGs on the growth of the human gastric carcinoma cell line KATO III were investigated. All the PGs tested inhibited KATO III cell growth with a relative potency order of PGE2 > PGE1 > 17S,20-dimethyl-6-oxo PGE1-methyl ester (ornoprostil) > PGF2α. This inhibition was accompanied by an increase of cyclic adenosine monophosphate production. Furthermore, in the presence of guanosine triphosphate, these PGs stimulated adenylate cyclase activity in the plasma membrane of KATO III cells, followed by enhancement of membrane guanosine triphosphatase activity. The relative potencies of these PGs for increasing cyclic adenosine monophosphate levels, activating adenylate cyclase, and enhancing guanosine triphosphatase activity were all comparable to those for inhibiting cell growth. On the other hand, the proliferation of KATO III cells was also inhibited by forskolin as well as dibutyryl cyclic adenosine monophosphate, whereas none of the agents that did not increase cyclic adenosine monophosphate levels had any effect. These results suggest that PGs inhibit KATO III cell growth by stimulating cyclic adenosine monophosphate production via a guanosine triphosphate-dependent process, suggesting the involvement of guanosine triphosphate-binding stimulatory protein, probably coupled to PGE2 receptors, in the action of PGs.

Intraluteal Infusions of Prostaglandins of the E, D, I, and A Series Prevent PGF2α-Induced, but Not Spontaneous, Luteal Regression in Rhesus Monkeys1

A luteotropic role for prostaglandins (PGs) during the luteal phase of the menstrual cycle of rhesus monkeys was suggested by the observation that intraluteal infusion of a PG synthesis inhibitor caused premature luteolysis. This study was designed to identify PGs that promote luteal function in primates. First, the effects of various PGs on progesterone (P) production by macaque luteal cells were examined in vitro. Collagenase-dispersed luteal cells from midluteal phase of the menstrual cycle (Day 6-7 after the estimated surge of LH, n = 3) were incubated with 0-5,000 ng/ml PGE2, PGD, 6 beta PGI1 (a stable analogue of PGI2), PGA2, or PGF2 alpha alone or with hCG (100 ng/ml). PGE2, PGD2, and 6 beta PGI1 alone stimulated (p less than 0.05) P production to a similar extent (2- to 3-fold over basal) as hCG alone, whereas PGA2 and PGF2 alpha alone had no effect on P production. Stimulation (p less than 0.05) of P synthesis by PGE2, PGD2, and 6 beta PGI1 in combination with hCG was similar to that of hCG alone. Whereas PGA2 inhibited gonadotropin-induced P production (p less than 0.05), that in the presence of PGF2 alpha plus hCG tended (p = 0.05) to remain elevated. Second, the effects of various PGs on P production during chronic infusion into the CL were studied in vivo. Saline with or without 0.1% BSA (n = 12), PGE2 (300 ng/h; n = 4), PGD2 (300 ng/h; n = 4), 6 beta PGI1 (500 ng/h; n = 3), PGA2 (300 ng/h; n = 4), or PGF2 alpha (10 ng/h; n = 8) was infused via osmotic minipump beginning at midluteal phase (Days 5-8 after the estimated LH surge) until menses. In addition, the same dose of PGE, PGD, PGI, or PGA was infused in combination with PGF2 alpha (n = 3-4/group) for 7 days. P levels over 5 days preceding treatment were not different among groups. In 5 of 8 monkeys receiving PGF2 alpha alone, P declined to less than 0.5 ng/ml within 72 h after initiation of infusion and was lower (p less than 0.05) than controls. The length of the luteal phase in PGF2 alpha-infused monkeys was shortened (12.3 +/- 0.9 days; mean +/- SEM, n = 8; p less than 0.05) compared to controls (15.8 +/- 0.5). Intraluteal infusion of PGE, PGD, PGI, or PGA alone did not affect patterns of circulating P or luteal phase length.(ABSTRACT TRUNCATED AT 400 WORDS)

Inhibition of human gingival carcinoma cell growth by prostaglandins

The inhibitory effects of various prostaglandins (PGA 2, PGD 2 and PGE 2) on the growth of human gingival carcinoma cell line Ca 9–22 and human cervical carcinoma cell line HeLa were studied in vitro. 1. 1. PGA 2 and PGD 2 significantly depressed Ca 9–22 cell proliferation in dose and time related fashion. 2. 2. The inhibitory rate by PGs for Ca 9–22 cells exceeded than HeLa-cells. 3. 3. IC 50 value of PGD 2 on growth of Ca 97ndash;22 was calculated to be 4 μg/ml.

Prostaglandins and their precursors can modify genetic damage-induced by gamma-radiation and benzo (a) pyrene

Experiments were performed to study the effect of various prostaglandins (PGs) and their precursors, gamma-linolenic acid (GLA) and arachidonic acid (AA) on gamma-radiation and benzo (a) pyrene (BP) -induced genetic damage to the bone marrow cells of mice, using the sensitive micronucleus (MN) test. Thromboxane B2 prostaglandin E1 and GLA completely prevented BP-induced and reduced to a great degree radiation-induced genetic damage. where as PGE2, PGF2alpha and AA were without any effect. Since GLA and AA are widely distributed in the cell membranes, and as PGs can be formed virtually in response to any type of stimulus., it is likely that GLA and PGE1 may function as endogenous anti-mutagenic chemicals.

The effects of PGF 1 α, PGE 2 and 16,16 dimethyl PGE 2 on gastric emptying and small intestinal transit in rat

Prostaglandins are well known for their ability to stimulate contraction in gastrointestinal smooth muscle, yet very little information is available on how their activity affects propulsion in vivo . Thus, studies were undertaken to determine the effect of various prostaglandins on qastric emptying (GE) and small intestinal transit (SIT) in unanesthetized fasted rats. Rats were treated with intravenous, subcutaneous, or oral PGF 2 α , PGE 2, or 16,16 dimethyl PGE 2 at various doses, followed 1 (intravenous), 20 (subcutaneous) or 10 (oral) mins later by intragastric 51Cr oxide in black ink. Forty-five mins later, rats were sacrificed by CO 2 asphyxiation, the pylorus clamped, and the gut excised. SIT was expressed as the percent of intestinal length traveled by the most distal portion of ink. GE was expressed as the percent of the 51Cr emptied into the intestines. If GE was affected by prostaglandin treatment, the experiments were repeated with rats pre-implanted with duodenal cannula. This preparation allowed the visual transit marker to be deposited directly into the dueodenum, thus avoiding acceleration or delay of SIT caused by fluctuations in GE. The results of these studies show that: (1) intravenous 16,16 dimethyl PGE 2 (5–50 μg/kg), but not PGF 2 α or PGE 2, accelerates GE and delays SIT; (2) oral prostaglandin administration increases SIT; (3) oral 16,16 dimethyl PGE 2 delays GE; (4) subcutaneous 16,16 dimethyl PGE 2 accelerates, has no effect upon, or delays GE depending upon dose, but accelerates SIT at all doses tested; and (5) subcutaneous PGE 2 accelerates SIT while PGF 2 α does not. Thus, the effect of prostaglandins on GE and SIT depends upon the dosage and route of administration as well as type of prostaglandin used.

Prostaglandin stimulation of ornithine decarboxylase activity in mammary gland explants from mid-pregnant mice

The effects of various prostaglandins on ornithine decarboxylase (ODC) activity in mammary gland explants from mid-pregnant mice have been tested. PGE 1, E 2 and I 2 elicit a concentration-dependent stimulation of ODC activity. The minimally effective concentrations are 0.5 ug/ml for PGE 1 and E 2, and 50 ug/ml for PGF 2α and 6-keto-PGF 1α. The PGE 1 effect had a time course identical to that of prolactin. The prolactin action on ODC activity was attentuated by indomethacin, an inhibitor of prostaglandin biosynthesis. Arachidonic acid stimulation ODC activity and its effect was abolished by indomethacin. The phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, potentiated the PGE 1 effect on ODC activity. The results suggest that the prostaglandins may modulate prolactin's action of ODC activity via a cAMP dependent mechanism.

プロスタグランディンによるキンギョＣａｒａｓｓｉｕｓ ａｕｒａｔｕｓのｉｎ ｖｉｔｒｏ排卵誘起効果

The in vitro effects of various prostaglandins (PGE1, PGE2, PGF1α and PGF2α) on ovulation were investigated in isolated goldfish Carassius auratus oocytes previously matured in vivo by injection of human chorionic gonadotropin. PGE1, PGE2, PGF1α and PGF2α all induced ovulation; PGF group was more effective than PGE group, PGF 2αbeing the most effective. Over 50% of oocytes underwent ovulation 15 to 30min after the beginning of incubation with PGF2αat a concentration of 1μg/ml; over 80% of oocytes ovulated within 1 hr. Observations of the ovulatory process in vitro were made using both dissecting microscope and scanning electron microscope. Oocytes from ovarian fragments were expelled into the incubation medium through a rupture in the follicle at the point corresponding to attachment to the overlying epithelium. In situ, the rupture at this point would allow the oocyte to be expelled directly into the ovarian lumen. Ovulation may be cause by contraction of the ovarian follicle layer.

Effects of some naturally occurring prostaglandins of the D-, E-, and I-type and synthetic analogues on adenylate cyclase of human fat cell ghosts

The effects of various prostaglandins originating from arachidonic acid (prostaglandin E2, D2, I2) as well as of methylated analogues of prostaglandin E2 (16,16-dimethyl prostaglandin E2 and 15-S-methyl prostaglandin E2) on the human fat cell adenylate cyclase were studied. In addition, the stable breakdown product of prostaglandin I2, prostaglandin 6-keto-F1-alpha, was tested for activity. Prostaglandin E2 and its methylated analogues as well as prostaglandin D2 and I2 were active stimulators of the human fat cell enzyme. The stable breakdown product of prostaglandin I2 (prostaglandin 6-keto-F1-alpha) which is biologically inactive had no stimulatory effects, suggesting that stimulation of the human fat cell function. The stimulatory action of prostaglandin D2 is consistent with the elevation of cAMP-levels induced by this compound in intact fat cells. It is concluded that the stimulatory effects of prostaglandins on the human fat cell adenylate cyclase are related to their stimulatory effects upon lipolysis.

The effect of various prostaglandins on plasma membrane receptors and function of mouse macrophages.

Mobility and redistribution of receptor molecules on the macrophage surface appear to be important for the interaction between macrophages and phagocytized particles and between macrophages and lymphocytes (1–3). It has been suggested that prostaglandins (PGs) may modulate the function of macrophages, since high doses (10−2–10−3 mg/ml) inhibited phagocytosis of SRC, whereas lower doses (10−8–10−4 mg/ml) enhanced phagocytosis (4). It was thus of interest to determine whether endogenous synthesis of PGs by the macrophage (5) is relevant in this process, and whether modulation by PGs is achieved by changing plasma membrane receptors. In this communication, we report that inhibition of PG synthesis in the macrophage interferes with phagocytosis and that PG treatment to macrophages leads to morphological changes in the membrane and to modulation of Con A and Fc cell membrane receptors.

Effect of various prostaglandins on the release of arachidonic acid from cultured fibroblasts

Effect of various prostaglandins on the release of arachidonic acid from [ 14C]arachidonic acid labeled fibroblasts was studied. Prostaglandin(PG) F 2α was found to enhance the release of radioactive arachidonic acid from the cells. The stimulatory effect was dose dependent, and was greater than that of bradykinin. The active compounds can be ranked in potency for the release of arachidonic acid from the pre-labeled cells per cent of control: PGF 2α(200.1%)>PGF 1α (141.8%)>PGD 2 (137.1%)>thromboxane B 2 (113.7%)>PGE 2 (109.4%). On the other hand, PGI 2 showed a strong inhibitory effect on the arachidonic acid release from the pre-labeled cells (the value was only 69% of the control), while 6-ketoPGF 1α, an end metabolite of PGI 2, had no effect.

Effect of prostaglandins on macromolecular transport from blood to lymph in the dog.

The effect of various prostaglandins on hindlimb lymph flow and macromolecular transport was studied in dogs anesthetized with pentobarbital sodium. Lymph obtained by cannulating the popliteal lymphatics was collected at 30-min intervals and analyzed for protein and exogenously administered dextran (Dextran 110). Arterial blood was obtained at the midpoint of each collection period and similarly analyzed. Prostaglandins (E1, E2, F2alpha, and A2), the vehicle and histamine were injected subcutaneously into the paw of the dog. Prostaglandins slightly increased lymph flow (L') but the lymph-to-plasma concentration ratios (R) for total protein (T) and Dextran 110 (D) decreased. Permeability surface area products (PS) were not altered. The sieving ratios (RD/RT) were substantially less than 1 and were not altered by prostaglandins. These results indicate that selective permeability of the capillary is not impaired by prostaglandins. Timing sequences and dose-response relations were also completed for prostaglandins by subcutaneous testing in dogs injected with Evans blue (T-1824). Leakage of the T-1824-albumin complex occurred when large amounts (migrogram) of prostaglandins were administered, and the response appeared to be short lived (less than 30 min). While the prostaglandins possess vasoactive properties, as demonstrated by an increased lymph flow, they do not alter the restrictive transport of large molecules.

Effect of prostaglandins on α-aminoisobutylic acid uptake in cultured fibroblasts

Effect of various prostaglandins on the uptake of α-aminoisobutylic acid by cultured fibroblasts was studied. All the prostaglandins having an OH functional group in an intramolecular 5-membered ring showed an inhibitory effect on the amino acid uptake. The active compounds can be ranked in potency according to the values for the inhibition of the amino acid uptake per cent of control: prostaglandin F 2α(53 %) >F 1α(54 %) >D 2(56 %) >E 2(62 %) >thromboxane B 2 (66 %). Thus, prostaglandin F 2α was found to be the most potent inhibitor to membrane permeability and the inhibitory effect was dose dependent. The inhibition was maximal after 1 hour of exposure to prostaglandin F 2α, persisted at least up to 6 hours in the presence of prostaglandin F 2α.

Stimulative effect of prostaglandins on production of hexosamine-containing substances by cultured fibroblasts (2) early effect of various prostaglandins at various doses

Early effects of various prostaglandins on the production of hexosamine-containing substances by cultured fibroblasts, which were derived from a rat carrageenin granuloma, were studied. At the stationary phase, the cells were exposed for 6 h to one of the prostaglandin A 1 (PGA 1), A 2, B 1, B 2, D 2, F 1α, F 2α, E 1, E 2 or arachidonic acid in various concentrations ranging from 0.01 to 10 μg/ml for all the stimuli and from 10 pg to 10 μg/ml for PGF 2α. The activity of the cells in incorporating 3H-glucosamine into hexosamine-containing substances (acidic) glycosaminoglycans and glycoproteins) during this period was compared with that of control cells. All the stimuli tested showed more or less stimulative effect on the synthesis of hexosamine-containing substances at their specific concentrations. PGF 2α was found to be the most potent stimulant and its stimulative effect was found significant even at the low concentration of 100 pg/ml. PGD 2, F 1α and E 2 were the next potent stimuli. Their optimum dose were around 1 μg/ml but they still had significant stimulation at the concentration of 0.01 μg/ml. Effect of PGE 2 was rather mild. Stimulation by PGA 1, A 2, B 1 and B 2 or arachidonic acid was seen at high dose, and its seemed to be non-specific. The results suggested that these prostaglandins such as PGF 2α, D 2, F 1α and E 2 play some important role on regulating the production of intercellular ground substances.